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A U-shaped relationship between birth weight and several components of the metabolic syndrome was confirmed in a contemporary, well-nourished Western population of full-term newborns, but post-natal weight gain was the dominant factor associated with the high-risk cluster. There was a prominence of higher as well as lowest birth weights in those at risk. Future health programs should focus on both pre- and post-natal factors (reducing excess childhood weight gain and smoking during pregnancy), and possibly the greatest benefits may arise from targeting the heaviest, as well as lightest newborns, especially with a history of maternal smoking during pregnancy.

The aetiology and management approach for cough in children differs greatly to that in adults, so the empirical approach commonly used in adults is unsuitable for children. Clinical evaluation of cough in children should include an assessment of environmental factors, particularly tobacco smoke, parental concerns and expectations. Most children with acute cough are likely to have an uncomplicated viral acute respiratory tract infection, but the possibility of a more serious problem, especially aspiration of foreign material, should always be considered. Isolated chronic cough in children is rarely asthma, and the term “cough variant asthma” should not be used. Over‐the‐counter and prescription medications are ineffective for the symptomatic relief of acute cough. Treatment for chronic cough should be based on aetiology. Because of the favourable natural history of cough, a “positive” response in medication trials should not be assumed to be due to the medication. Children should be reassessed within the expected timeframe of response to therapy.

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Wheeze persisting from ages 6 to 18 years is associated with multiple factors, including reduced infant lung function, infant-onset atopy, maternal asthma, and active smoking. Wheeze at age 18 years (regardless of previous wheeze status) is associated with active smoking, but only among those with reduced lung function in infancy. These findings give unique insight into the cause of obstructive airways disease in 18-year-olds, and follow-up of this cohort might be expected to further extend our understanding.

Objective To compare the prevalence and management of asthma before and after institution of the National Asthma Campaign. Design Repeat population‐based cross‐sectional analytic surveys. Setting Eastern Australia (Sydney, Brisbane, Melbourne, and the Hunter Valley, New South Wales) in September 1990 and 1993. Subjects Primary school children and their parents from 33 schools (8746 children) in 1990 and 40 schools (10106 children) in 1993. Outcome measures Frequency of respiratory symptoms; diagnoses of asthma; medications; lung function measurements; possession of a peak flow meter and a written action plan. Results Age and sex distribution of the subjects and the reported prevalence of asthma were similar in 1990 and 1993. The frequency of reported episodes of wheezing and troublesome cough increased significantly in children between 1990 and 1993. Asthma management improved in accordance with current recommendations, with significantly decreased use of regular inhaled bronchodilator medication in children and increased use of preventive medication, monitoring of lung function by doctors and use of peak flow meters and written action plans in both children and adults. Conclusion There is evidence that the National Asthma Campaign may have contributed to increased awareness and improved management of asthma in children and adults in eastern Australia.

Background Associations between Clara cell secretory protein gene variants (SCGB1A1, also known as CC16, CC10, CCSP and uteroglobin) and the asthma phenotype have been found in five out of eight studies world-wide. No study has investigated the contribution of SCGB1A1 polymorphisms to the development and/or persistence of the asthma phenotype in a birth cohort followed over time.Objective The aim of this study was to determine the role of the SCGB1A1 gene in the development of the asthma phenotype. Methods The Perth Infant Asthma Follow-up (PIAF) cohort (n = 231 unrelated infants, unselected for asthma and recruited at birth) were seen at 1 month, 6 and 11 years of age, and had a questionnaire, lung function, airway responsiveness (AR) and skin prick tests (SPTs) completed. Blood was taken at 6 and 11 years for total and specific immunoglobulin E (sIgE) and DNA extraction. SPT positivity had at least one positive SPT. SIgE44 kU/L had at least one sIgE above 4 kU/L. SCGB1A1 A38G (rs3741240), that alters gene transcription, was genotyped using Sau96I restriction digestion of exon 1 PCR products. Results At 6 and 11 years of age, 33.0% and 29.7% of those genotyped had doctor-diagnosed asthma, and 35.8% and 52.1% had SPT positivity. In cross-sectional analyses, children with 38G/38A or 38A/38A had increased AR at 1 month (1.72-fold, P = 0.013); sIgE44 kU/L [odds ratio (OR) = 6.95, 95% confidence interval (CI) = 1.35-35.91, P = 0.021]; house dust mite (HDM) SPT positivity (OR = 7.21, 95% CI = 1.09-47.78, P = 0.041) and sIgE (4.57-fold, P = 0.045) at 6 years; and doctor-diagnosed asthma (OR = 3.93, 95% CI = 1.24-12.47, P = 0.02) and cat SPT positivity (OR = 4.34, 95% CI = 1.01-18.77, P = 0.049) at 11 years. Longitudinal analyses of 6 and 11 years paired data showed that children with 38A/38A had increased persistent sIgE44 kU/L (OR = 11.87, 95% CI = 1.97-71.53, P = 0.007) and persistent HDM SPT positivity (OR = 7.84, 95% CI = 1.04-58.92, P = 0.045). Conclusion SCGB1A1 A38G may play a role in the development and persistence of the asthma phenotype in childhood.